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TCR deep sequencing of transgenic RAG ‐1‐deficient mice reveals endogenous TCR recombination: a cause for caution
Author(s) -
McGuire Helen M,
Watkins Thomas S,
Field Matthew,
Taylor Sarah,
Yasuyama Nao,
Farmer Andrew,
Miles John J,
Fazekas de St. Groth Barbara
Publication year - 2018
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1111/imcb.12033
Subject(s) - t cell receptor , transgene , genetically modified mouse , biology , endogeny , gene knockout , knockout mouse , microbiology and biotechnology , gene , t cell , genetics , biochemistry , immune system
The utility of T‐cell receptor ( TCR ) transgenic mice in medical research has been considerable, with applications ranging from basic biology all the way to translational and clinical investigations. Crossing of TCR transgenic mice with either recombination‐activating gene (RAG)‐1 or RAG ‐2 knockouts is frequently used to generate mice with a monoclonal T‐cell repertoire. However, low level productive TCR rearrangement has been reported in RAG ‐deficient mice expressing transgenic TCR s. Using deep sequencing, we set out to directly examine and quantify the presence of these endogenous TCR s. Our demonstration that functional nontransgenic TCR s are present in nonmanipulated mice has wide reaching ramifications worthy of critical consideration.